| Gastric cancer is a disease that serious threat to human health and life. Many epidemiological studies have shown that Helicobacter pylori (H.pylori, HP) is closely related to gastric cancer. The gastric mucosa will follow to the chronic gastritis, gastric ulcer, gastric cancer pathological changes when gastric mucosa is infected by HP. HP has been formulated class I gastric carcinogen by WHO in 1994. HP in a gastric cancer-related research provides a new means of prevention. However, epidemiological data alone is no longer in-depth understanding of the relationship between HP and gastric cancer. As medical science develops, we pay more attention to the research of HP causative agents, vaccines, and its molecular mechanism of gastric carcinogenesis.At present, a variety of animals are used to produce animal models through inoculating HP, including pigs, cats, ferrets, monkeys, mice and Mongolian gerbils and so on. The Mongolian gerbil is considered the most stable model of gastric cancer induced by Helicobacter pylori infection in animal models.Modern research confirms that glycyrrhizic acid and its derivatives are important and effective ingredient in licorice having anti-inflammatory, anti-ulcer, anti-tumor and enhancing immune function and so on. The 18β-glycyrrhetinic acid has the strongest pharmacological activity in the series of glycyrrhizic acid and its derivatives. European scholars of the studies have shown that glycyrrhizic acid and its derivatives significantly increased the intragastric volume of free mucus and gastric mucus and promote gastric mucosal synthesis of PGE2 and increased gastric mucosal blood flow, and thus play a good anti-inflammatory, anti-ulcer treatment effect. The vitro experiments designed by German Rea Krausse in 2007 demonstrated that the growth of glycyrrhizin on HP had a certain inhibitory effect. But there is no report of in vivo experiment until now.In this study, we establish an animal model through H. pylori infection in Mongolian gerbils and to study the role of anti-HP infection and the mechanism of 18β-glycyrrhetinic acid. The Mongolian gerbils were divided into four groups, namely, the blank control group, simple infections HP pathological model group, HP infection and restrained by amoxicillin, clarithromycin and esomeprazole triple drug control group, HP infection and restrained by 18β-glycyrrhetinic acid group. We have studied the impact of 18β-glycyrrhetinic acid on HP infected Mongolian gerbils through the general shape specimen study, gastric PH value test, HE staining pathological examination, as well as gastric tissue specimens by immunohistochemical.The pathological examination showed significant inflammatory mucosal changes in infection rate was 100% in the HP infection model group. There is no significant inflammatory changes in HP infection adds 18β-glycyrrhetinic acid group and no significant difference with the blank group and HP infection plus triple drug control group. At the same time gastric tissue Ki-67 immuno- histochemical staining confirmed that 18β-glycyrrhetinic acid significantly inhibited the cell proliferation. All of these have proved that 18β-glycyrrhetinic acid can inhibit the HP colonization in the gastric mucosa, inhibit inflammation and proliferation and have no significant difference with the commonly clinical used amoxicillin, clarithromycin and esomeprazole triple treatment. In this study, we successful establish the chronic gastritis animal model of HP infection in Mongolian gerbils and prove that 18β-glycyrrhetinic acid have a certain inhibition for HP infection in vivo experiment for the first time.Therefore, this experiment can provide a reference drug for clinical prevention and treatment of HP infection and the primary prevention for gastric cancer.Objective: To establish the chronic gastritis animal model of HP infection in Mongolian gerbils and to study the role and mechanism of 18β-glycyrrhetinic acid resist HP infection.Methods: The standard strain ATCC43504 with H. pylori infection in Mongolian gerbils. Mongolian gerbils were divided into four groups, namely, the blank control group, simple infections HP pathological model group, HP infection and restrained by amoxicillin, clarithromycin and esomeprazole triple drug control group, HP infection and restrained by 18β-glycyrrhetinic acid group. To study the impact of 18β-glycyrrhetinic acid on HP infected Mongolian gerbils through the general shape specimen study, gastric PH value test, HE staining pathological examination, as well as gastric tissue specimens by immunohistochemical.Results: The pathological examination showed significant inflammatory mucosal changes in infection rate was 100% in the HP infection model group. There is no significant inflammatory changes in HP infection adds 18β- glycyrrhetinic acid group and no significant difference with the blank group and HP infection plus triple drug control group. At the same time gastric tissue Ki-67 immunohistochemical staining confirmed that 18β-glycyrrhetinic acid signi- ficantly inhibited the cell proliferation.Conclusions:Established a stable recovery and culture system for HP; successful established the chronic gastritis animal model of HP infection in Mongolian gerbils; for follow-up experiments HP infection in the molecular mechanism of gastric mucosal lesions and gastric cancer-related research laid a solid foundation; confirmed chronic HP infection can promote the expression of Ki-67, leading to the occurrence of gastric mucosal lesions; for the first time in vivo experiments confirmed the use of 18β-glycyrrhetinic acid can inhibit bacterial growth, reduce inflammation and cell proliferation. |
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